the substance deposited in skin and sclera in jaundice is
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Jaundice
Jaundice, also known as hyperbilirubinemia,[1] is a yellow discoloration of the body tissue resulting from the accumulation of an excess of bilirubin. Deposition of bilirubin happens only when there is an excess of bilirubin, a sign of increased production or impaired excretion. The normal serum levels of bilirubin are less than 1mg/dl; however, the clinical presentation of jaundice as scleral icterus (peripheral yellowing of the eye sclera), is best appreciated only when the levels reach more than 3 mg/dl. Sclerae have a high affinity for bilirubin due to their high elastin content.[2] With further increase in serum bilirubin levels, the skin will progressively discolor ranging from lemon yellow to apple green, especially if the process is long-standing; the green color is due to biliverdin.[3]
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Jaundice
Abel Joseph; Hrishikesh Samant.
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Last Update: August 8, 2022.
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Continuing Education Activity
Jaundice, also known as hyperbilirubinemia, is defined as a yellow discoloration of the body tissue resulting from the accumulation of excess bilirubin. Deposition of bilirubin happens only when there is an excess of bilirubin, and this indicates increased production or impaired excretion. The normal serum levels of bilirubin are less than 1 milligram per deciliter (mg/dL). However, the clinical presentation of jaundice with peripheral yellowing of the eye sclera, also called scleral icterus, is best appreciated when serum bilirubin levels exceed 3 mg/dl. With further increase in serum bilirubin levels, the skin will progressively discolor ranging from lemon yellow to apple green, especially if the process is long-standing; the green color is due to biliverdin. This activity reviews the evaluation and differential diagnosis of jaundice and highlights the role of an interprofessional team in evaluating and improving care for patients with this condition.
Objectives:Describe the etiology and pathophysiology of jaundice.
Outline the approach to performing a history and physical examination for patients with jaundice.
Summarize the treatment and management options available for patients with jaundice.
Explain the interprofessional team strategies for improving care coordination to advance the management of jaundice and improve outcomes.
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Introduction
Jaundice, also known as hyperbilirubinemia,[1] is a yellow discoloration of the body tissue resulting from the accumulation of an excess of bilirubin. Deposition of bilirubin happens only when there is an excess of bilirubin, a sign of increased production or impaired excretion. The normal serum levels of bilirubin are less than 1mg/dl; however, the clinical presentation of jaundice as scleral icterus (peripheral yellowing of the eye sclera), is best appreciated only when the levels reach more than 3 mg/dl. Sclerae have a high affinity for bilirubin due to their high elastin content.[2] With further increase in serum bilirubin levels, the skin will progressively discolor ranging from lemon yellow to apple green, especially if the process is long-standing; the green color is due to biliverdin.[3]
Bilirubin has two components: unconjugated(indirect) and conjugated(direct), and hence elevation of any of these can result in jaundice. Icterus acts as an essential clinical indicator for liver disease, apart from various other insults.[4]
Yellowing of skin sparing the sclerae is indicative of carotenoderma which occurs in healthy individuals who consume excessive carotene-rich foods.[5]
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Etiology
CONJUGATED HYPERBILIRUBINEMIA[6]Dubin-Johnson syndrome
Rotor syndrome
Hepatocellular disease - Viral hepatitis A, B, D; alcoholic hepatitis; cirrhosis, nonalcoholic steatohepatitis, EBV, CMV, HSV, Wilson, autoimmune
Cholestatic liver disease-Primary biliary cholangitis, primary sclerosing cholangitis
Infiltrative diseases (e.g., amyloidosis, lymphoma, sarcoidosis, tuberculosis)
Sepsis and hypoperfusion states
Total parenteral nutrition
Drugs & Toxins - oral contraceptives, rifampin, probenecid, steroids, chlorpromazine, herbal medications (e.g., Jamaican bush tea, kava kava), arsenic
Hepatic crisis in sickle cell disease
Pregnancy
Choledocholithiasis
Tumors (e.g., cholangiocarcinoma, head of pancreas cancer)
Extrahepatic biliary atresia
Acute and chronic pancreatitis
Strictures
Parasitic infections (e.g., Ascaris lumbricoides, liver flukes)
UNCONJUGATED HYPERBILIRUBINEMIAHemolytic anemias, extravasation of blood in tissues, dyserythropoiesis
Gilbert syndrome [10]
Crigler–Najjar syndrome type 1 and 2
Hyperthyroid Estrogen Go to:
Epidemiology
The prevalence of jaundice differs among patient populations; newborns and elderly more commonly present with the disease.[12]
The causes of jaundice also vary with age, as mentioned above. Around 20 percent of term babies are found with jaundice in the first week of life, primarily due to immature hepatic conjugation process.[13] Congenital disorders, overproduction from hemolysis, defective bilirubin uptake, and defects in conjugation are also responsible for jaundice in infancy or childhood. Hepatitis A was found to be the most afflicting cause of jaundice among children.[14][15] Bile duct stones, drug-induced liver disease, and malignant biliary obstruction occur in the elderly population.
Men have an increased prevalence of alcoholic and non-alcoholic cirrhosis, chronic hepatitis B, malignancy of pancreas, or sclerosing cholangitis.[16] In contrast, women demonstrate higher rates of gallbladder stones, primary biliary cirrhosis, and gallbladder cancer.[17]
Kernicterus or Bilirubin-induced neurologic dysfunction (BIND), a complication of severe jaundice is a very rare cause of death in neonates with a death rate of 0.28 deaths per one million live births.[18]
Jaundice
Jaundice
jaundice (evidence of liver disease) leading to portal hypertension
From: Lanzkowsky's Manual of Pediatric Hematology and Oncology (Seventh Edition), 2022
Related terms:
BilirubinDiarrheaAbdominal PainAnemiaLiver DiseaseLiver InjuryHepatitisLiver CirrhosisCholestasis
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Manifestations of Liver Disease
Robert M. Kliegman MD, in Nelson Textbook of Pediatrics, 2020
Jaundice (Icterus)
Yellow discoloration of the sclera, skin, and mucous membranes is a sign of hyperbilirubinemia (seeChapter 123.3). Clinically apparent jaundice in children and adults occurs when the serum concentration of bilirubin reaches 2-3 mg/dL (34-51 µmol/L); the neonate might not appear jaundiced until the bilirubin level is >5 mg/dL (>85 µmol/L). Jaundice may be the earliest and only sign of hepatic dysfunction. Liver disease must be suspected in the infant who appears only mildly jaundiced but has dark urine or acholic (light-colored) stools. Immediate evaluation to establish the cause is required.
Measurement of the total serum bilirubin concentration allows quantitation of jaundice. Bilirubin occurs in plasma in 4 forms:unconjugated bilirubin tightly bound to albumin;free orunbound bilirubin (the form responsible for kernicterus, because it can cross cell membranes);conjugated bilirubin (the only fraction to appear in urine); andδ fraction (bilirubin covalently bound to albumin), which appears in serum when hepatic excretion of conjugated bilirubin is impaired in patients with hepatobiliary disease. The δ fraction permits conjugated bilirubin to persist in the circulation and delays resolution of jaundice. Although the termsdirect andindirect bilirubin are used equivalently withconjugated andunconjugated bilirubin, this is not quantitatively correct, because the direct fraction includes both conjugated bilirubin and δ bilirubin.
Investigation of jaundice in an infant or older child must include determination of the accumulation of both unconjugated and conjugated bilirubin. Unconjugated hyperbilirubinemia might indicate increased production, hemolysis, reduced hepatic removal, or altered metabolism of bilirubin (Table 382.2). Conjugated hyperbilirubinemia reflects decreased excretion by damaged hepatic parenchymal cells or disease of the biliary tract, which may be a result of obstruction, sepsis, toxins, inflammation, and genetic or metabolic disease (Table 382.3).
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Jaundice
Steven McGee MD, in Evidence-Based Physical Diagnosis (Fourth Edition), 2018
A Jaundice
Jaundice is usually first noted in the eyes, but the traditional term for this finding (scleral icterus) is actually a misnomer because pathologic studies reveal most of the pigment to be deposited in the conjunctiva, not the avascular sclera.3 As jaundice progresses and the serum bilirubin increases, the face, mucous membranes, and eventually the entire skin acquire a yellow or orange hue.
Prominent yellowish subconjunctival fat may be mistaken for conjunctival jaundice, but fat is usually limited to the conjunctival folds and, unlike jaundice, spares the area near the cornea. Patients with carotenemia (from excess carrot or multivitamin ingestion) also develop a yellowish discoloration of the skin, especially the palms, soles, and nasolabial fold, but in contrast to jaundice, the conjunctiva are spared.4
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Approach to the Patient with Jaundice or Abnormal Liver Tests
Lee Goldman MD, in Goldman-Cecil Medicine, 2020
Approach to the Patient With Hyperbilirubinemia
Hyperbilirubinemia and jaundice may result from isolated disorders of bilirubin metabolism, liver disease, or obstruction of the biliary tract. Jaundice represents the most visible sign of hepatobiliary disease of many causes (Table 138-1).
Genetic Disorders of Bilirubin Conjugation
The hereditary hyperbilirubinemias (Table 138-2) are a group of five syndromes in which hyperbilirubinemia occurs as an isolated biochemical abnormality, without evidence of either hepatocellular necrosis or cholestasis.
Crigler-Najjar and Gilbert Syndromes
Crigler-Najjar syndrome types 1 and 2 and Gilbert syndrome are hereditary forms of unconjugated hyperbilirubinemia that have been known for more than two decades to result principally from mutations inUGT1A1. In Crigler-Najjar type 1, essentially no functional enzyme activity is present, whereas patients with Crigler-Najjar type 2 have up to 10% of normal and patients with Gilbert syndrome have 10 to 33% of normal activity, leading to bilirubin concentrations of 18 to 45, 6 to 25, and 1.5 to 4 mg/dL, respectively (seeTable 138-2). Because total UGT1A1 enzymatic activity must be reduced to less than 50% of normal to produce unconjugated hyperbilirubinemia, phenotypic expression of mutations in this enzyme requires either homozygosity or double heterozygosity, and each of these disorders is inherited as an autosomal recessive trait. Most cases of Crigler-Najjar types 1 and 2 also arise from homozygous or double heterozygous structural mutations within the coding region. In Western countries, patients with Gilbert syndrome are typically homozygous for an A(TA)7TAA promoter mutation; this polymorphism is designatedUGT1A1∗28. Structural mutations in exon 1 ofUGT1A1 causing modest reductions in UGT1A1 enzymatic activity havebeen reported in some Japanese patients with Gilbert syndrome. To date, at least 130 different mutations inUGT1A1 associated with hereditary hyperbilirubinemia have been identified, including ones linked to Crigler-Najjar type 1 and type 2. Other studies in patients with unconjugated hyperbilirubinemia have also identified mutations and polymorphism in multiple additional regions ofUGT1A including its promoter region, in the solute carrier protein SCLO1B1, and in the enzymes heme oxygenase and biliverdin reductase A that influence serum bilirubin concentrations.2 The resulting complex genotypes may pose a risk not only for hyperbilirubinemia but also for susceptibility to glucuronidation-associated drug toxicity and, perhaps, for subtle diverse benefits as well.
Why does a jaundiced person's eyes and skin look yellow?
... asks JANANI from Chennai
India Elections World Opinion Today's Paper
Why does a jaundiced person's eyes and skin look yellow?
... asks JANANI from Chennai
June 17, 2015 11:46 pm | Updated June 18, 2015 04:16 am IST
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PROF DR V NAGARAAJAN , Madurai, Tamil Nadu, answers...There are two types of bile pigments, both are yellow in colour, one being Bilirubin, and the other, Biliverdin. These two pigments impart colour to the bile salts, which are called glycocholate, and taurocholate.
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